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We previously demonstrated that the survival time of BALB/c mice challenged with Toxoplasma gondii RH strain was prolonged by immunising the mice with a eukaryotic vector expressing the protein ROP16 of T. gondii. Building upon previous findings, we are exploring improved vaccination strategies to enhance protection. In this work, a novel recombinant canine adenovirus type 2 expressing ROP16 (CAV-2-ROP16) of T. gondii was constructed and identified to express ROP16 in Madin-Darby canine kidney cells (MDCK) cells by western blot (WB) and indirect immunofluorescence (IFA) assays. Intramuscular immunisation of BALB/c mice with CAV-2-ROP16 was performed to evaluate the humoral and cellular immune responses. This vaccination triggered significant humoral and cellular responses, including ROP16-stimulated lymphoproliferation (P0.05). Compared to control groups, the CAV-2-ROP16 immunised mice had high production of IFN-γ, IL-2 and IL-12 (P0.05), with a predominance of IgG2a production, but not IL-10 (P0.05), revealing that a predominant Th1-type response had developed. The cell-mediated cytotoxic activity with high levels of IFN-γ and TNF-α was significantly increased in both CD4

The aim of our study was to detect differentially regulated proteins and specific signaling pathways in Mongolian gerbil brains during chronic Toxoplasma gondii (T.gondii) PRU strain infection. We use a iTRAQ-based strategy to detecte 4935 proteins, out of which 110 proteins were differentially expressed (/=2.0-fold, p value0.05) when the brain of gerbils infected with T.gondii was compared to control brain tissues. We confirmed the authenticity and the accuracy of iTRAQ results through quantitative real-time PCR and western blot (WB), which was consistent with mass spectrometry analysis. Pathway analysis and GO (Gene Ontology) annotations indicated the deregulation of several pathways related to immune response, metabolism and neurological processes, like neuronal growth and neurotransmitter transport. Through the iTRAQ-based strategy, we obtained a comparative proteome profile of brain tissues from Mongolian gerbils with chronic infection of T.gondii. Several differentially expressed proteins involved in neurological pathways, like Parvalbumin, Drebrin or Synaptotagmin, can be further investigated to enhance our understanding of central nervous system (CNS) injury caused by T.gondii.T.gondii can infect almost all nucleated cells with a preference for the CNS, which can induce Toxoplasma encephalitis (TE). However, the pathogenesis and mechanisms between the parasite and host associated with TE are largely unexplored. Around 30% of the world population is considered to have latent infection with T.gondii and90% patients died of TE, while the proportion of secondary paralysis is also high. Patients of TE may have highly varied neurological symptoms with both focal and diffuse neurological lesions, while mental symptoms and behavior disorders are frequently accompanied, like the Alzheimer's disease (AD). We present a comparative proteomics analysis to explore the differences of protein expression caused by chronic T.gondii infection. The results of this analysis can be helpful for identifying key proteins involved in the pathogenesis of TE. In addition, the study can contribute to a better understanding of molecular mechanisms underlying the host-parasite relationship in chronic infection of T.gondii and facilitate further development of new therapies for TE.